PF-562271 (besylate)
Based on 32 publication(s) in Google Scholar
PF-562271 besylate (VS-6062 besylate) is an orally active, ATP-competitive, reversible FAK/Pyk2 inhibitor, with an IC50 of 1.5 nM for FAK and 13 nM for Pyk2. PF-562271 besylate induces tumor regression, and inhibits tumor growth, invasion and metastasis. PF-562271 besylate exerts no effect on tumor necrosis, angiogenesis or apoptosis in an orthotopic mouse model of pancreatic ductal adenocarcinoma. When combined with Sunitinib (HY-10255A), PF-562271 besylate reduces tumor vascularization, decreases serum alpha-fetoprotein levels and improves cachexia. PF-562271 besylate can be used in research related to prostate cancer, breast cancer, pancreatic cancer, colon cancer, glioblastoma, lung cancer, pancreatic ductal adenocarcinoma and hepatocellular carcinoma.
For research use only. We do not sell to patients.
- Purity: 99.17%
- CAS No.: 939791-38-5
- Formula: C27H26F3N7O6S2
- Molecular Weight:665.66
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Storage:
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Publications Citing Use of MedChemExpress (MCE) PF-562271 (besylate)
More- Nat Biomed Eng. 2025 Nov 3. [Abstract]
- Cancer Res. 2013 May 1;73(9):2873-83. [Abstract]
- Autophagy. 2026 May 29:1-15. [Abstract]
- Cell Discov. 2022 Sep 6;8(1):84. [Abstract]
- Sci Transl Med. 2018 Jul 18;10(450):eaaq1093. [Abstract]
- Carbohydr Polym. 2024 Feb 15:326:121637. [Abstract]
- Cell Death Dis. 2023 Feb 24;14(2):157. [Abstract]
- Cell Death Dis. 2022 Sep 10;13(9):783. [Abstract]
- Clin Cancer Res. 2019 Jul 15;25(14):4552-4566. [Abstract]
- Int J Surg. 2025 Sep 17. [Abstract]
- Am J Chin Med. 2025;53(4):1225-1240. [Abstract]
- World J Gastroenterol. 2025 Jul 28;31(28):107361. [Abstract]
- Cell Rep. 2023 Oct 5;42(10):113213. [Abstract]
- Life Sci. 2021 Apr 1:270:119112. [Abstract]
- Breast Cancer Res. 2024 Mar 19;26(1):48. [Abstract]
- Sci Rep. 2018 May 8;8(1):7228. [Abstract]
- Int J Cancer. 2015 Oct 1;137(7):1549-59. [Abstract]
- Cell Signal. 2025 Sep 10:136:112117. [Abstract]
- Environ Toxicol Pharmacol. 2023 Nov:104:104301. [Abstract]
- Eur J Cell Biol. 2024 May 28;103(2):151427. [Abstract]
- Cancer Med. 2025 Sep;14(18):e71227. [Abstract]
- Mol Biol Rep. 2026 May 14;53(1):770. [Abstract]
- Mol Biol Rep. 2025 May 14;52(1):458. [Abstract]
- J Nat Med. 2020 Sep;74(4):732-740. [Abstract]
- Anticancer Drugs. 2024 Jan 1;35(1):46-54. [Abstract]
- Res Sq. 2025 Jul 11.
- University of Washington. 2025.
- bioRxiv. 2025 May 28.
- bioRxiv. 2025 Apr 7:2025.04.01.646098. [Abstract]
- Research Square Preprint. 2023 May 23.
- Research Square Preprint. 2021 Dec.
- Practical Oncology Journal. 2015, 29(5): 444-449.
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Biological Activity
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| A549 | GI50 |
2.1 μM
Compound: PF-562271
|
Antiproliferative activity against human A549 cells after 2 days by spectrophotometric analysis
Antiproliferative activity against human A549 cells after 2 days by spectrophotometric analysis
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[PMID: 30340900] |
| HeLa | GI50 |
1.7 μM
Compound: PF-562271
|
Antiproliferative activity against human HeLa cells after 2 days by spectrophotometric analysis
Antiproliferative activity against human HeLa cells after 2 days by spectrophotometric analysis
|
[PMID: 30340900] |
| HepG2 | GI50 |
1.2 μM
Compound: PF-562271
|
Antiproliferative activity against human HepG2 cells after 2 days by spectrophotometric analysis
Antiproliferative activity against human HepG2 cells after 2 days by spectrophotometric analysis
|
[PMID: 30340900] |
| OVCAR-3 | GI50 |
1.8 μM
Compound: PF-562271
|
Antiproliferative activity against human OVCAR3 cells after 2 days by spectrophotometric analysis
Antiproliferative activity against human OVCAR3 cells after 2 days by spectrophotometric analysis
|
[PMID: 30340900] |
| U-87MG ATCC | GI50 |
3.7 μM
Compound: PF-562271
|
Antiproliferative activity against human U87MG cells after 2 days by spectrophotometric analysis
Antiproliferative activity against human U87MG cells after 2 days by spectrophotometric analysis
|
[PMID: 30340900] |
PF-562271 besylate potently inhibits purified recombinant FAK (with an IC50 of 1.5 nM) and recombinant Pyk2 (with an IC50 of 13 nM) via ATP-competitive reversible binding[1].
PF-562271 besylate exhibits over 100-fold selectivity against most tested non-target recombinant kinases, and only shows moderate activity against a subset of cyclin-dependent kinase complexes[1].
PF-562271 (starting concentration of 1 μM; 30 min) besylate potently and suppresses the autophosphorylation of FAKY397 in A431 epithelial cancer cells with an IC50 of 5 nM[1].
PF-562271 (1.1-3.3 μM; 48 h) besylate alters the cell cycle progression of PC-3M cells only after incubation at the high concentration of 3.3 μM for 48 h[1].
PF-562271 besylate is an ATP-competitive reversible inhibitor that potently inhibits the kinase activities of purified recombinant FAK (IC50 = 1.5 nM) and PYK2 (IC50 = 14 nM)[2].
PF-562271 (0.1 μM) besylate significantly inhibits IGF-I-stimulated chemotactic migration of the PDA cell line MPanc-96, but does not affect EGF-stimulated migration of this cell line[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:Inducible stable A431 epithelial carcinoma clones expressing wild-type V5-tagged FAK
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Concentration:1 μmol/L (starting concentration, serially diluted)
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Incubation Time:30 min
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Result:Inhibited FAKY397 autophosphorylation with an IC50 of 5 nmol/L (2.5 ng/mL).
Showed ~4-fold lower potency for Pyk2 in comparative cell assays.
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Cell Line:PC-3M human prostate cancer cells
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Concentration:1.1 μmol/L; 3.3 μmol/L
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Incubation Time:48 h
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Result:Reduced the percentage of cells in S and G2-M phases to levels comparable to serum-starved cells at 3.3 μmol/L.
Exerted no effect on cell cycle progression at 1.1 μmol/L.
PF-562271 (25-50 mg/kg; p.o.; once daily, twice daily; 15 days) besylate induces dose-dependent tumor growth inhibition in PC-3M xenografts. The efficacy of twice-daily administration is superior to that of once-daily administration at the same total daily dose, and the dose of 50 mg/kg twice daily achieves a TGI of 78% accompanied by partial tumor regression[1].
PF-562271 (50-100 mg/kg; p.o.; twice daily, once daily; continuous delivery via osmotic minipump) besylate induces significant tumor growth inhibition in BxPc3 xenografts, with the 50 mg/kg twice daily dose achieving 86% TGI and partial tumor regression[1].
PF-562271 (12.5-50 mg/kg; p.o.; twice daily; for 29 consecutive days) besylate induces dose-dependent tumor growth inhibition in BT474 xenografts, with the 50 mg/kg twice-daily dose achieving a 94% TGI accompanied by partial tumor regression[1].
PF-562271 (33 mg/kg; twice daily) besylate reduces tumor volume, decreases tumor cell proliferation rate, and significantly lowers the incidence of retroperitoneal invasion and metastasis of orthotopic MPanc-96 pancreatic ductal adenocarcinoma in athymic nude mice[2].
Combination treatment with PF-562271 (15 mg/kg; p.o.; twice daily; 7 days per week) besylate and Sunitinib (HY-10255A) administered at 20 mg/kg four times daily effectively inhibits hepatocellular carcinoma tumor growth in nude mice, reduces serum AFP and AST levels, impairs tumor angiogenesis, and induces tumor necrosis[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:CD-1 Nu/Nu (female, ≈20 grams, U87MG human glioblastoma xenograft model)[1]
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Dosage:3.3 mg/kg; 10 mg/kg; 33 mg/kg
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Administration:p.o.; single dose
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Result:Achieved 78% maximal inhibition of tumor phospho-FAK at 1 hour postdose, with >50% inhibition sustained for >4 hours (33 mg/kg dose).
Achieved 70% maximal inhibition of tumor phospho-FAK, with >50% inhibition sustained for <2 hours (10 mg/kg dose).
Calculated an EC50 of 93 ng/mL for total blood PF-562271 (mesylate) concentration required for half-maximal reduction of FAK phosphorylation.
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Animal Model:CD-1 Nu/Nu (female, ≈20 grams, PC-3M human prostate xenograft model)[1]
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Dosage:50 mg/kg (daily); 25 mg/kg (twice daily); 50 mg/kg (twice daily)
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Administration:p.o.; daily; 15 days; p.o.; twice daily; 15 days
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Result:Resulted in 45% tumor growth inhibition (TGI) and 37% inhibition of tumor phospho-FAK after 15 days, with a free Cₘₐₓ of 157 ng/mL (50 mg/kg daily dose).
Resulted in 61% TGI and 27% inhibition of tumor phospho-FAK after 15 days, with a free Cₘₐₓ of 25 ng/mL (25 mg/kg twice daily dose).
Resulted in 78% TGI, 52% inhibition of tumor phospho-FAK after 15 days, regressions in 3/7 mice, a free Cₘₐₓ of 96 ng/mL, and a free Cₐᵥₑ of 16 ng/mL (50 mg/kg twice daily dose).
Caused no weight loss, morbidity, or mortality.
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Animal Model:CD-1 Nu/Nu (female, ≈20 grams, BxPc3 human pancreatic xenograft model)[1]
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Dosage:50 mg/kg (twice daily); 100 mg/kg (daily); steady-state free concentration of 0.7 ng/mL (continuous delivery)
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Administration:p.o.; twice daily; p.o.; daily; continuous delivery via osmotic mini-pump
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Result:Resulted in 86% TGI, 31% inhibition of tumor phospho-FAK, regressions in 3/10 mice, and a free Cₘₐₓ of 273 ng/mL (50 mg/kg twice daily dose).
Resulted in 71% TGI and 59% inhibition of tumor phospho-FAK, with a free Cₘₐₓ of 705 ng/mL (100 mg/kg daily dose).
Resulted in 57% TGI and 37% inhibition of tumor phospho-FAK (continuous delivery via osmotic mini-pumps).
Caused no weight loss, morbidity, or mortality.
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Animal Model:CD-1 Nu/Nu (female, ≈20 grams, BT474 human breast xenograft model)[1]
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Dosage:12.5 mg/kg (twice daily); 25 mg/kg (twice daily); 50 mg/kg (twice daily)
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Administration:p.o.; twice daily; 29 days
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Result:Resulted in 37% TGI, 50% inhibition of tumor phospho-FAK, a free Cₘₐₓ of 29 ng/mL, and a free Cₐᵥₑ of 3 ng/mL (12.5 mg/kg twice daily dose).
Resulted in 59% TGI, 55% inhibition of tumor phospho-FAK, regressions in 3/8 mice, a free Cₘₐₓ of 116 ng/mL, and a free Cₐᵥₑ of 14 ng/mL (25 mg/kg twice daily dose).
Resulted in 94% TGI, 76% inhibition of tumor phospho-FAK, regressions in 4/8 mice, a free Cₘₐₓ of 180 ng/mL, and a free Cₐᵥₑ of 40 ng/mL (50 mg/kg twice daily dose).
Caused no weight loss, morbidity, or mortality.
Chemical Information
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CAS No. 939791-38-5
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Appearance Solid
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Molecular Weight 665.66
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Formula C27H26F3N7O6S2
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Color Off-white to light yellow
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SMILES
CS(=O)(N(C)C1=NC=CC=C1CNC2=NC(NC3=CC4=C(NC(C4)=O)C=C3)=NC=C2C(F)(F)F)=O.O=S(C5=CC=CC=C5)(O)=O
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Synonyms
VS-6062 (besylate)
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Publications (32)
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Journal Impact Factor
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Most Recent
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Nat Biomed Eng
Nonexpansive biodegradable matrix promotes blood vessel organoid development for neurovascular repair and functional recovery in ischaemic stroke. [Abstract]2025 Nov 3. PMID: 41184604 -
Cancer Res
High-throughput tyrosine kinase activity profiling identifies FAK as a candidate therapeutic target in Ewing sarcoma. [Abstract]2013 May 1;73(9):2873-83. PMID: 23536552
PF-562271 (besylate) purchased from MedChemExpress. Usage Cited in: Cancer Res. 2013 May 1;73(9):2873-83. [Abstract]
FAK inhibition downregulates the AKT/mTOR pathway and CAS activity. A, protein levels measured by Western immunoblotting for AKT/mTOR pathway proteins in A673 and TC32 cells serum-starved overnight, treated with PF-562271 for 6 hours, and then stimulated with IGF-1 for 2 hours. Vinculin is used as the loading control. B, Western immunoblots showing downregulation of phospho-CAS but not phospho-ERK in A673 and TC32 cells after treatment with PF-562271.
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Autophagy
PTK2/FAK inhibition triggers TMED9-mediated protective autophagy in pancreatic cancer cell via enhancing ERGIC-ERES contact. [Abstract]2026 May 29:1-15. PMID: 42144738 -
Cell Discov
A positive mechanobiological feedback loop controls bistable switching of cardiac fibroblast phenotype. [Abstract]2022 Sep 6;8(1):84. PMID: 36068215 -
Sci Transl Med
PP2A inhibition is a druggable MEK inhibitor resistance mechanism in KRAS-mutant lung cancer cells. [Abstract]2018 Jul 18;10(450):eaaq1093. PMID: 30021885 -
Carbohydr Polym
Inulin-like polysaccharide ABWW may impede CCl4 induced hepatic stellate cell activation through mediating the FAK/PI3K/AKT signaling pathway in vitro & in vivo. [Abstract]2024 Feb 15:326:121637. PMID: 38142102 -
Cell Death Dis
Identification of matrix-remodeling associated 5 as a possible molecular oncotarget of pancreatic cancer. [Abstract]2023 Feb 24;14(2):157. PMID: 36828810
PF-562271 (besylate) purchased from MedChemExpress. Usage Cited in: Cell Death Dis. 2023 Feb 24;14(2):157. [Abstract]
PF-562271 (250 nM; 6 h) largely inhibits Akt-S6 phosphorylation in OE-MXRA5 priPC-1 cells.
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Cell Death Dis
P130cas-FAK interaction is essential for YAP-mediated radioresistance of non-small cell lung cancer. [Abstract]2022 Sep 10;13(9):783. PMID: 36088346 -
Clin Cancer Res
High-throughput Chemical Screening Identifies Focal Adhesion Kinase and Aurora Kinase B Inhibition as a Synergistic Treatment Combination in Ewing Sarcoma. [Abstract]2019 Jul 15;25(14):4552-4566. PMID: 30979745 -
Int J Surg
Supervising the recurrence of pancreatic ductal adenocarcinoma using CtDNA-based MIR129-2 methylation detection. [Abstract]2025 Sep 17. PMID: 40961228 -
Am J Chin Med
Evodiamine Suppresses Lung Cancer Progression Through Modulating FAK/STAT3/AKT Signaling Pathway. [Abstract]2025;53(4):1225-1240. PMID: 40582716 -
World J Gastroenterol
FBP1 as a key regulator of focal adhesion kinase-mediated hepatic stellate cell activation: Multi-omics and experimental validation. [Abstract]2025 Jul 28;31(28):107361. PMID: 40741470 -
Cell Rep
Mechanotransduction in response to ECM stiffening impairs cGAS immune signaling in tumor cells. [Abstract]2023 Oct 5;42(10):113213. PMID: 37804510 -
Life Sci
Harmine inhibits the proliferation and migration of glioblastoma cells via the FAK/AKT pathway. [Abstract]2021 Apr 1:270:119112. PMID: 33508300 -
Breast Cancer Res
TMEM120B strengthens breast cancer cell stemness and accelerates chemotherapy resistance via β1-integrin/FAK-TAZ-mTOR signaling axis by binding to MYH9. [Abstract]2024 Mar 19;26(1):48. PMID: 38504374 -
Sci Rep
The mechanical microenvironment regulates ovarian cancer cell morphology, migration, and spheroid disaggregation. [Abstract]2018 May 8;8(1):7228. PMID: 29740072 -
Int J Cancer
2015 Oct 1;137(7):1549-59. PMID: 25809490
PF-562271 (besylate) purchased from MedChemExpress. Usage Cited in: Int J Cancer. 2015 Oct 1;137(7):1549-59. [Abstract]
786-O (a) and Caki-1 (b) are treated for 24 and 48h with increasing concentrations of PF-562,271 and adherent cells were counted. Cell lysates are evaluated through immunoblotting for total FAK following treatment for 24h.
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Cell Signal
Tenvermectin B, a novel macrocyclic lactone antibiotic, suppresses glioblastoma progression by targeting RhoJ. [Abstract]2025 Sep 10:136:112117. PMID: 40939916 -
Environ Toxicol Pharmacol
ZC3H4 Governs Epithelial Cell Migration through ROCK/p-PYK2/p-MLC2 Pathway in Silica-induced Pulmonary Fibrosis. [Abstract]2023 Nov:104:104301. PMID: 37866415 -
Eur J Cell Biol
The mechanical mechanism of angiotensin II induced activation of hepatic stellate cells promoting portal hypertension. [Abstract]2024 May 28;103(2):151427. PMID: 38820882 -
Cancer Med
Focal Adhesion Kinase Intersects With the BRD4-MYC Axis and YAP1 to Drive Tumor Cell Growth, Phenotypic Plasticity, Stemness, and Metastatic Potential in Colorectal Cancer. [Abstract]2025 Sep;14(18):e71227. PMID: 40959971 -
Mol Biol Rep
Piperlongumine inhibits the proliferation and migration of non-small cell lung cancer cells through the EGFR/FAK/STAT3 pathway. [Abstract]2026 May 14;53(1):770. PMID: 42133146 -
Mol Biol Rep
Ginkgetin inhibits the proliferation and migration of lung cancer cells via FAK/STAT3/AKT pathway. [Abstract]2025 May 14;52(1):458. PMID: 40366441 -
J Nat Med
2020 Sep;74(4):732-740. PMID: 32643027 -
Anticancer Drugs
2024 Jan 1;35(1):46-54. PMID: 37449977 -
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bioRxiv
2025 Apr 7:2025.04.01.646098. PMID: 40291676 -
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PF-562271 (besylate) purchased from MedChemExpress. Usage Cited in: Practical Oncology Journal. 2015, 29(5): 444-449.
Effects and mechanism of Biglycan and FAK signaling pathway on the invasion and metastasis of colon cancer cells.
Solvent & Solubility
DMSO : 21.4 mg/mL (32.15 mM; Need ultrasonic and warming; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
H2O : < 0.1 mg/mL (insoluble)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 1.67 mg/mL (2.51 mM); Clear solution
This protocol yields a clear solution of ≥ 1.67 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (16.7 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 1.67 mg/mL (2.51 mM); Clear solution
This protocol yields a clear solution of ≥ 1.67 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (16.7 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL. * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Purity & Documentation
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Data Sheet (290 KB)
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SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
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Handling Instructions (2659 KB)
References
[1]. Roberts WG, et al. Antitumor activity and pharmacology of a selective focal adhesion kinase inhibitor, PF-562,271. Cancer research. 2008 Mar 15;68(6):1935-44. [Content Brief]
[2]. Stokes JB, et al. Inhibition of focal adhesion kinase by PF-562,271 inhibits the growth and metastasis of pancreatic cancer concomitant with altering the tumor microenvironment. Molecular cancer therapeutics. 2011 Nov;10(11):2135-45. [Content Brief]
[3]. Bagi CM, et al. Sunitinib and PF-562,271 (FAK/Pyk2 inhibitor) effectively block growth and recovery of human hepatocellular carcinoma in a rat xenograft model. Cancer biology & therapy. 2009 May;8(9):856-65. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 1.5023 mL | 7.5113 mL | 15.0227 mL | 37.5567 mL |
| 5 mM | 0.3005 mL | 1.5023 mL | 3.0045 mL | 7.5113 mL | |
| 10 mM | 0.1502 mL | 0.7511 mL | 1.5023 mL | 3.7557 mL | |
| 15 mM | 0.1002 mL | 0.5008 mL | 1.0015 mL | 2.5038 mL | |
| 20 mM | 0.0751 mL | 0.3756 mL | 0.7511 mL | 1.8778 mL | |
| 25 mM | 0.0601 mL | 0.3005 mL | 0.6009 mL | 1.5023 mL | |
| 30 mM | 0.0501 mL | 0.2504 mL | 0.5008 mL | 1.2519 mL |